Rittinger K, Budman J, Xu J, Volinia S, Cantley L C, Smerdon S J, Gamblin S J, Yaffe M B
Divison of Protein Structure, National Institute for Medical Research, London, United Kingdom.
Mol Cell. 1999 Aug;4(2):153-66. doi: 10.1016/s1097-2765(00)80363-9.
We have solved the high-resolution X-ray structure of 14-3-3 bound to two different phosphoserine peptides, representing alternative substrate-binding motifs. These structures reveal an evolutionarily conserved network of peptide-protein interactions within all 14-3-3 isotypes, explain both binding motifs, and identify a novel intrachain phosphorylation-mediated loop structure in one of the peptides. A 14-3-3 mutation disrupting Raf signaling alters the ligand-binding cleft, selecting a different phosphopeptide-binding motif and different substrates than the wild-type protein. Many 14-3-3: peptide contacts involve a C-terminal amphipathic alpha helix containing a putative nuclear export signal, implicating this segment in both ligand and Crm1 binding. Structural homology between the 14-3-3 NES structure and those within I kappa B alpha and p53 reveals a conserved topology recognized by the Crm1 nuclear export machinery.
我们解析了与两种不同磷酸丝氨酸肽结合的14-3-3的高分辨率X射线结构,这两种肽代表了不同的底物结合基序。这些结构揭示了所有14-3-3亚型中肽与蛋白质相互作用的进化保守网络,解释了两种结合基序,并在其中一种肽中鉴定出一种新型的链内磷酸化介导的环结构。破坏Raf信号传导的14-3-3突变改变了配体结合裂隙,选择了与野生型蛋白不同的磷酸肽结合基序和不同底物。许多14-3-3与肽的接触涉及一个包含假定核输出信号的C末端两亲性α螺旋,表明该片段参与配体和Crm1结合。14-3-3核输出信号结构与IκBα和p53中的结构之间的结构同源性揭示了Crm1核输出机制识别的保守拓扑结构。